ESTRO 2023 - Abstract Book

S420

Sunday 14 May 2023

ESTRO 2023

Conclusion The present analysis showed for the first time the benefit of adding PRSi Cox-NTCP prediction models. These models allow both a patient-specific tailoring of prediction and accounting of follow-up time. All models were based on a large modern multicenter prospective cohort with long term standardised follow-up. REQUITE was funded from the European Union's 7th FP GA 601826. RADprecise was funded by the ERA PerMed Network Reference Number: ERAPERMED2018-244. OC-0511 Hypoxic tumour cells drive tumour relapse after radiotherapy as revealed by a novel tracing tool A. Menegakis 1,2 , C. Vennin 3 , J. Ient 4 , R. Klompmaker 2 , L. Krenning 2 , A. Friskes 2 , M. ilic 2 , R. Harkes 5 , A. Groot 4 , J. van Rheenen 3 , M. Vooijs 4 , R. Medema 2 1 Netherlands Cancer Institute (NKI), Radiation Oncology, Amsterdam, The Netherlands; 2 Netherlands Cancer Institute (NKI), Cell Biology, Amsterdam, The Netherlands; 3 Netherlands Cancer Institute (NKI), Molecular Pathology, Amsterdam, The Netherlands; 4 GROW School for Oncology and Developmental Biology, Maastricht University Medical Centre, Radiation Oncology (Maastro), Maastricht, The Netherlands; 5 Netherlands Cancer Institute (NKI), Bioimaging facility, Amsterdam, The Netherlands Purpose or Objective Tumour hypoxia imposes a main obstacle to the efficacy of anti-cancer therapy, especially for radiotherapy and represents an important negative prognostic factor for treatment outcome and tumour progression of most solid tumours. Understanding the cellular dynamics of individual hypoxic cells prior, during and post-treatment will be of critical importance to understand their role in tumour progression and relapse. Materials and Methods Here, we use H1299 lung adenocarcinoma cells expressing a novel lineage-tracing reporter of hypoxic cells to study the fate of this population after irradiation in tumor spheroids and in xenografts by means of multiphoton microscopy, flow cytometry analysis and immunofluorescence. Lineage tracing relies on the expression of a HIF1a-CreERT2-UnaG reporter (H1299-UnaG cells), which upon treatment with tamoxifen drives the sustained expression of UnaG in HIF1a-expressing cells.

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